ArticleThe American journal of pathology2005
Virus-specific antibody, in the absence of T cells, mediates demyelination in mice infected with a neurotropic coronavirus.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- PART 2: Mouse models for multiple sclerosis research.Neurourology and urodynamics · 2021Review
- Oligodendrocytes that survive acute coronavirus infection induce prolonged inflammatory responses in the CNS.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Coronaviruses and Central Nervous System Manifestations.Frontiers in neurology · 2020Review
- Multiple sclerosis: experimental models and reality.Acta neuropathologica · 2017Review
- Infections and multiple sclerosis.Handbook of clinical neurology · 2014Review
- Role for complement in the development of seizures following acute viral infection.Journal of virology · 2010Article
- Protective and pathologic roles of the immune response to mouse hepatitis virus type 1: implications for severe acute respiratory syndrome.Journal of virology · 2009Article
- Coronaviruses post-SARS: update on replication and pathogenesis.Nature reviews. Microbiology · 2009Review
- Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2.Journal of virology · 2008Article
- Maturation and localization of macrophages and microglia during infection with a neurotropic murine coronavirus.Brain pathology (Zurich, Switzerland) · 2008Article
- Anti-viral T-cell immunity+anti-CNS autoantibody=a model for human acute disseminated encephalomyelitis or multiple sclerosis relapse?The American journal of pathology · 2007Article
- Pathogenesis of acute and chronic central nervous system infection with variants of mouse hepatitis virus, strain JHM.Immunologic research · 2007Review
- Functional diversity of chemokines and chemokine receptors in response to viral infection of the central nervous system.Current topics in microbiology and immunology · 2006Review
- Immunopathogenesis of coronavirus infections: implications for SARS.Nature reviews. Immunology · 2005Review
- A severe acute respiratory syndrome-associated coronavirus-specific protein enhances virulence of an attenuated murine coronavirus.Journal of virology · 2005Article
- Viral expression of CCL2 is sufficient to induce demyelination in RAG1-/- mice infected with a neurotropic coronavirus.Journal of virology · 2005Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mice infected with mouse hepatitis virus strain JHM develop an inflammatory demyelinating disease in the central nervous system with many similarities to human multiple sclerosis. The mouse disease is primarily immune-mediated because demyelination is not detected in JHM-infected mice lacking T or B cells but does occur after transfer of JHM-specific T cells. Although less is known about the ability of antibodies to mediate demyelination, the presence of oligoclonally expanded B cells and high concentrations of antibodies (against self or infectious agents) in the central nervous system of many multiple sclerosis patients suggests that antibodies may also contribute to myelin destruction. Here, we show that anti-JHM antibodies, in the absence of T or B cells, caused demyelination in JHM-infected mice. Anti-JHM antibody was detected adjacent to areas of demyelination, consistent with a direct interaction between antibody and infected cells. Demyelination was reduced by 85 to 90% in infected RAG1(-/-) mice lacking normal expression of activating Fc receptors (FcRgamma(-/-)) and by approximately 76% when complement was depleted by treatment with cobra venom factor. These data demonstrate that JHM-specific antibodies are sufficient to cause demyelination and that myelin destruction in the presence of anti-virus antibodies results from a combination of complement- and Fc receptor-dependent mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.